The present invention relates to methods and apparatuses for monitoring biological parameters, and in particular to a method and apparatus for measuring cardiac function in a subject using bioelectric impedance or components of bioelectric impedance.
The reference to any prior art in this specification is not, and should not be taken as, an acknowledgment or any form of suggestion that the prior art forms part of the common general knowledge.
It is estimated that coronary heart disease will become the single biggest public health problem in the world by 2020, The treatment of coronary heart disease and other cardiovascular diseases therefore represents and increasingly large health and economic burden throughout the world in the coming years.
Cardiac output (CO), which can be defined as the amount of blood ejected by the ventricles of the heart per minute (measured in liters per minute), is governed by the metabolic demands of the body, and therefore reflect the status of the entire circulatory system. For this reason measurement of cardiac output is an essential aspect of haemodynamic monitoring of patients with heart disease or who are recovering from various forms of cardiovascular disease or other medical treatments.
One existing technique for determining cardiac function which has been developed is known as impedance cardiography (IC). Impedance cardiography involves measuring the electrical impedance of a subject's body using a series of electrodes placed on the skin surface. Changes in electrical impedance at the body's surface are used to determine changes in tissue volume that are associated with the cardiac cycle, and accordingly, measurements of cardiac output and other cardiac function.
A complication in impedance cardiography is that the baseline impedance of the thorax varies considerably between individuals, the quoted range for an adult is 20 Ω-48 Ω at a frequency between 50 kHz-100 kHz. The changes in impedance due to the cardiac cycle are a relatively small (0.5%) fraction of the baseline impedance, which leads to a very fragile signal with a low signal to noise ratio.
Accordingly, complex signal processing is required to ensure measurements can be interpreted.
An example of this is described in international patent publication no. WO2004/032738, In this example, the responsiveness of a patient to an applied current is modelled using the equivalent circuit shown in FIG. 1. The equivalent circuit assumes that:                direct current is conducted through the extracellular fluid only since the reactance of the cell membrane will be infinite;        an applied alternating current is conducted through the extracellular and intracellular pathways in a ratio dependent on the frequency of the applied signal.        
Accordingly, the equivalent circuit includes an intracellular branch formed from a capacitance C representing the capacitance of the cell membranes in the intracellular pathway and the resistance R1 representing the resistance of the intracellular fluid. The circuit also includes an extracellular branch formed from resistance RE which represents the conductive pathway through the tissue.
WO2004/032738 operates based on the assumption that the cardiac cycle will only have an impact on the volume of extracellular fluid in the patient's thorax, and therefore that cardiac function can be derived by considering changes in the extracellular component of the impedance. This is achieved by applying an alternating current at a number of different frequencies. The impedance is measured at each of these frequencies and then extrapolated to determine the impedance at zero applied frequency, which therefore corresponds to the resistance RE. This is then determined to be solely due to the extracellular fluid component and hence can be used to determine attributes of cardiac function, such as stroke volume.
However, in practice the impedance at zero frequency would not be due solely to extracellular fluids but would be influenced by a number of other factors. In particular, cells do not act as a perfect capacitor and accordingly, the intracellular fluid will contribute to the impedance at a zero applied frequency.
A further issue in WO2004/032738 is that the process determines the impedance at zero applied frequency using the “Cole model”. However, again this assumes idealised behaviour of the system, and consequently does not accurately model a subject's bioimpedance response. Consequently cardiac parameters determined using these techniques tend to be of only limited accuracy.